Activity of the α9α10 nAChR inversely correlates with the magnitude of acoustic injury

BOERO L; GOUTMAN J; ELGOYHEN AB; GOMEZ CASATI ME

Congreso; XXX Congreso Anual de la Sociedad Argentina de Investigación en Neurociencia; 2015

Noise induced hearing loss (NIHL) is a major public health problem. Here, we intend to address the role of the efferent olivocochlear system in NIHL. We made use of a murine model of enhanced noise protection, the Chrna9L9?T knock-in (KI), a mouse in which the α9 nicotinic receptor subunit bears a mutation and leads to enhanced medial efferent activity and a mouse model lacking the 9 subunit of the nicotinic receptor (Chrna9 knockout (KO)). We exposed WT, Chrna9L9?T KI and α9 KO mice to loud sounds (1-16 kHz, 100 dB SPL, 1hr) and measured auditory brainstem responses (ABR), which reflect synchronized discharges from neurons along the auditory pathway. We also tested outer hair cell function by recording the distortion product otoacoustic emissions (DPOAEs). Acoustic trauma produced large auditory threshold shifts in WT and Chrna9 KO mice one day after exposure. However, one week later, thresholds returned to normal in WT, whereas in the Chrna9 KO they did not recover. In contrast, Chrna9L9?T KI mice were resistant to the same noise exposure. Suprathreshold ABR amplitudes were reduced in both WT and Chrna9 KO mice 1 day and a week after exposure, suggesting an irreversible loss of cochlear nerve synapses, but the Chrna9L9?T KI mice showed no changes following noise trauma. Finally, we used immunohistochemistry to visualize efferent neurons and found disorganized terminals after trauma. These findings will contribute to the understanding of the role of the efferent system.